Bottom Line:
In males, ethanol exposure during the 1st, 2nd or 3rd trimester equivalent did not significantly reduce LTP in the DG.In females, ethanol exposure during either the 1st or 2nd trimester equivalents did not impact LTP in early adulthood, but following exposure during the 3rd trimester equivalent alone, LTP was significantly increased in the female DG.These results further exemplify the disparate effects between the ability to elicit LTP in the male and female brain following perinatal ethanol exposure (PNEE).

ABSTRACTFetal alcohol spectrum disorders occur when a mother drinks during pregnancy and can greatly influence synaptic plasticity and cognition in the offspring. In this study we determined whether there are periods during brain development that are more susceptible to the effects of ethanol exposure on hippocampal synaptic plasticity. In particular, we evaluated how the ability to elicit long-term potentiation (LTP) in the hippocampal dentate gyrus (DG) was affected in young adult rats that were exposed to ethanol during either the 1st, 2nd, or 3rd trimester equivalent. As expected, the effects of ethanol on young adult DG LTP were less severe when exposure was limited to a particular trimester equivalent when compared to exposure throughout gestation. In males, ethanol exposure during the 1st, 2nd or 3rd trimester equivalent did not significantly reduce LTP in the DG. In females, ethanol exposure during either the 1st or 2nd trimester equivalents did not impact LTP in early adulthood, but following exposure during the 3rd trimester equivalent alone, LTP was significantly increased in the female DG. These results further exemplify the disparate effects between the ability to elicit LTP in the male and female brain following perinatal ethanol exposure (PNEE).

brainsci-03-01076-f001: The effects of perinatal ethanol exposure (PNEE) during specific trimester equivalents on long-term potentiation (LTP) in the dentate gyrus (DG) of young adult male rats. PNEE during either the 1st (A), 2nd (B), or 3rd (C) trimester equivalents does not result in a significant reduction in DG LTP. (D) Summary of LTP results calculated by assessing the initial phase of the excitatory post-synaptic potentiation (EPSP) slope (10%–80%) at 55–60 min post-theta burst stimulation (TBS). Results are presented as means ± SEM and were considered statistically significant when p < 0.05.

Mentions:
In male offspring, a one-way ANOVA for perinatal condition (control, pair-fed1, pair-fed2, pair-fed3, ethanol1, ethanol2, ethanol3) revealed that there was no significant effect of perinatal condition on LTP [F(6, 53) = 0.601, p = 0.728; Figure 1]. Additionally, when the results for each trimester equivalent were analysed individually, 3 out of 8 males that were exposed to ethanol during the 1st trimester equivalent alone showed less than 30% LTP, whereas 2 out of 8 males that were exposed to ethanol during the 2nd trimester equivalent alone showed less than 30% LTP (data not shown). This is in contrast to ad libitum control males, pair-fed males and 3rd trimester equivalent ethanol-exposed males, where no animals showed less than 30% LTP. However, additional statistical analysis of each individual trimester equivalent failed to reveal any significant effects of perinatal condition during either the 1st [F(2, 20) = 1.63, p = 0.22], 2nd [F(2, 20) = 0.96, p = 0.40] or 3rd [F(2, 19) = 0.12, p = 0.89] trimester equivalent exposure groups. These results indicate that overall, ethanol exposure during a single trimester equivalent is not enough to cause reliable long-term deficits in LTP in the male DG.

brainsci-03-01076-f001: The effects of perinatal ethanol exposure (PNEE) during specific trimester equivalents on long-term potentiation (LTP) in the dentate gyrus (DG) of young adult male rats. PNEE during either the 1st (A), 2nd (B), or 3rd (C) trimester equivalents does not result in a significant reduction in DG LTP. (D) Summary of LTP results calculated by assessing the initial phase of the excitatory post-synaptic potentiation (EPSP) slope (10%–80%) at 55–60 min post-theta burst stimulation (TBS). Results are presented as means ± SEM and were considered statistically significant when p < 0.05.

Mentions:
In male offspring, a one-way ANOVA for perinatal condition (control, pair-fed1, pair-fed2, pair-fed3, ethanol1, ethanol2, ethanol3) revealed that there was no significant effect of perinatal condition on LTP [F(6, 53) = 0.601, p = 0.728; Figure 1]. Additionally, when the results for each trimester equivalent were analysed individually, 3 out of 8 males that were exposed to ethanol during the 1st trimester equivalent alone showed less than 30% LTP, whereas 2 out of 8 males that were exposed to ethanol during the 2nd trimester equivalent alone showed less than 30% LTP (data not shown). This is in contrast to ad libitum control males, pair-fed males and 3rd trimester equivalent ethanol-exposed males, where no animals showed less than 30% LTP. However, additional statistical analysis of each individual trimester equivalent failed to reveal any significant effects of perinatal condition during either the 1st [F(2, 20) = 1.63, p = 0.22], 2nd [F(2, 20) = 0.96, p = 0.40] or 3rd [F(2, 19) = 0.12, p = 0.89] trimester equivalent exposure groups. These results indicate that overall, ethanol exposure during a single trimester equivalent is not enough to cause reliable long-term deficits in LTP in the male DG.

Bottom Line:
In males, ethanol exposure during the 1st, 2nd or 3rd trimester equivalent did not significantly reduce LTP in the DG.In females, ethanol exposure during either the 1st or 2nd trimester equivalents did not impact LTP in early adulthood, but following exposure during the 3rd trimester equivalent alone, LTP was significantly increased in the female DG.These results further exemplify the disparate effects between the ability to elicit LTP in the male and female brain following perinatal ethanol exposure (PNEE).

ABSTRACTFetal alcohol spectrum disorders occur when a mother drinks during pregnancy and can greatly influence synaptic plasticity and cognition in the offspring. In this study we determined whether there are periods during brain development that are more susceptible to the effects of ethanol exposure on hippocampal synaptic plasticity. In particular, we evaluated how the ability to elicit long-term potentiation (LTP) in the hippocampal dentate gyrus (DG) was affected in young adult rats that were exposed to ethanol during either the 1st, 2nd, or 3rd trimester equivalent. As expected, the effects of ethanol on young adult DG LTP were less severe when exposure was limited to a particular trimester equivalent when compared to exposure throughout gestation. In males, ethanol exposure during the 1st, 2nd or 3rd trimester equivalent did not significantly reduce LTP in the DG. In females, ethanol exposure during either the 1st or 2nd trimester equivalents did not impact LTP in early adulthood, but following exposure during the 3rd trimester equivalent alone, LTP was significantly increased in the female DG. These results further exemplify the disparate effects between the ability to elicit LTP in the male and female brain following perinatal ethanol exposure (PNEE).